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Nature 451, 1066-1067 (28 February 2008) | doi:10.1038/4511066a; Published online 27 February 2008
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John Innes Centre Project Leader in Plant or Microbial Sciences
- University of East Anglia
- Norwich, NR4 7TJ, UK
Academic Surgical Pathologists GI / Breast / GYN
- Medical College of Wisconsin
- Milwaukee, Wisconsin, USA
Cancer: Crossing over to drug resistance
David M. Livingston1 & Daniel P. Silver1
Abstract
Certain cancers stem from mutations that prevent a cell from repairing its damaged DNA efficiently. But antitumour chemotherapy that exploits that repair defect can in turn be nullified by counter-mutation.
Two papers1, 2 in this issue provide insight into a subset of breast and ovarian cancers, the action of drugs used to treat them, and a novel mechanism of chemotherapeutic drug resistance. The papers are by Edwards et al.1 and Sakai et al.2, and appear on pages 1111 and 1116.
- David M. Livingston and Daniel P. Silver are at the Dana-Farber Cancer Institute, Harvard Medical School, 44 Binney Street, Boston, Massachusetts 02115, USA.
Email: david_livingston@dfci.harvard.edu
Email: daniel_silver@dfci.harvard.edu
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